Heat stress can have large effects on most aspects of reproductive function in mammals. These include disruptions in spermatogenesis and oocyte development, oocyte maturation, early embryonic development, foetal and placental growth and lactation. These deleterious effects of heat stress are the result of either the hyperthermia associated with heat stress or the physiological adjustments made by the heat-stressed animal to regulate body temperature. Many effects of elevated temperature on gametes and the early embryo involve increased production of reactive oxygen species. Genetic adaptation to heat stress is possible both with respect to regulation of body temperature and cellular resistance to elevated temperature.

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Effects of heat stress on mammalian reproduction.

http://animal.ifas.ufl.edu/hansen/publications_pdf/docs/2007_hansen_2.pdf

Exploitation of genetic and physiological determinants of embryonic resistance to elevated temperature to improve embryonic survival in dairy cattle during heat stress

Reduced reproductive performance of lactating cows during the summer is associated with decreased thermoregulatory competence due to intensive genetic selection for high milk production. This review examines the immediate and delayed effects of heat stress on follicular function and describes some potential strategies for their alleviation. It focuses on how heat stress affects the follicle and its enclosed oocyte, suggesting that perturbations in the follicular microenvironment, to which the oocytes are exposed for long periods of development, reduce their developmental competence. Among the potential alterations are reduction in gonadotropin secretion, alteration in follicular growth, attenuation of dominance, and disruption of steroidogenesis. Evaporative cooling methods are the most common strategy used to alleviate the effect of heat stress; however, there is a compelling need to find additional ways to improve fertility during the summer and autumn. Hormonal treatment to enhance removal of the impaired follicles by synchronization of follicular waves with GnRH and PGF2 alpha is suggested. An alternative method is stimulation of follicular growth by a brief treatment with bST or FSH. Other strategies, such as timed AI and embryo transfer, have been recently used, making the optimization of embryo cryopreservation procedures highly relevant. Protection of the ovarian pool of oocytes from thermal stress via nutritional manipulations or administration of antioxidants or other survival factors should also be considered. A better understanding of the underlying mechanisms by which heat stress impairs fertility may lead to the development of additional approaches to alleviate these effects.

Heat Stress, the Follicle, and Its Enclosed Oocyte: Mechanisms and Potential Strategies to Improve Fertility in Dairy Cows

Heat stress during the summer disrupts several reproductive processes, resulting in a pronounced depression of conception rate in dairy cows worldwide. The rise of internal body temperature during the summer is responsible for the impaired reproduction. A major cause for sustained hyperthermia during the summer is high milk production, which continues to rise. The processes of milk synthesis and secretion increase cows’ metabolic heat production. For instance, heat production of cows yielding 30 kg/day milk is twice as high as maintenance heat production of nonlactating cows, and that of high milk yielding cows giving 55 kg/day is about three times higher than maintenance heat production. Maintenance of normal and constant body temperature requires a balance between endogenous heat produced in the body and the amount of heat lost from the body to the environment. When heat production exceeds heat loss, the body temperature rises. Body temperatures of high milk yielding cows located in a wet region were found to start rising exponentially at air temperatures of 26–27 °C. Thus, even a small rise in air temperature, on the order of 1–2 °C, due, for instance, to global warming, may induce severe hyperthermia in dairy cows. This is clearly seen in Figure 1, which demonstrates the depressive effect of summer heat on the conception rate of lactating cows artificially inseminated (AI) in the summer months over the last 18 years to as low as 27.7%, compared with 42.6% during the cool winter months. Moreover, the “slightly” more severe conditions during the summers of 2010, 2012, and 2015, about 1.5 °C above average summer air temperatures, further decreased conception by an additional 5% units (Figure 1).

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Impact of heat stress on cow reproduction and fertility.

Among the components of the female reproductive tract, the ovarian pool of follicles and their enclosed oocytes are highly sensitive to hyperthermia. Heat-induced alterations in small antral follicles can be expressed later as compromised maturation and developmental capacity of the ovulating oocyte. This review summarizes the most up-to-date information on the effects of heat stress on the oocyte with an emphasis on unclear points and open questions, some of which might involve new research directions, for instance, whether preantral follicles are heat resistant. The review focuses on the follicle-enclosed oocytes, provides new insights into the cellular and molecular responses of the oocyte to elevated temperature, points out the role of the follicle microenvironment, and discusses some mechanisms that might underlie oocyte impairment. Mechanisms include nuclear and cytoplasmic maturation, mitochondrial function, apoptotic pathways, and oxidative stress. Understanding the mechanism by which heat stress compromises fertility might enable development of new strategies to mitigate its effects.

Effect of Heat Stress on Reproduction in Dairy Cows: Insights into the Cellular and Molecular Responses of the Oocyte.

Elevated temperature (heat stress) in vitro reduces androstenedione and estradiol and increases progesterone secretion by follicular cells from bovine dominant follicles.

M.A. Brusie

Papers

Elevated temperature (heat stress) in vitro reduces androstenedione and estradiol and increases progesterone secretion by follicular cells from bovine dominant follicles.